LncRNA-MIF, a c-Myc-activated long non-coding RNA, suppresses glycolysis by promoting Fbxw7-mediated c-Myc degradation.
Pengfei ZhangLimian CaoPingsheng FanYide MeiMian WuPublished in: EMBO reports (2016)
The c-Myc proto-oncogene is activated in more than half of all human cancers. However, the precise regulation of c-Myc protein stability is unknown. Here, we show that the lncRNA-MIF (c-Myc inhibitory factor), a c-Myc-induced long non-coding RNA, is a competing endogenous RNA for miR-586 and attenuates the inhibitory effect of miR-586 on Fbxw7, an E3 ligase for c-Myc, leading to increased Fbxw7 expression and subsequent c-Myc degradation. Our data reveal the existence of a feedback loop between c-Myc and lncRNA-MIF, through which c-Myc protein stability is finely controlled. Additionally, we show that the lncRNA-MIF inhibits aerobic glycolysis and tumorigenesis by suppressing c-Myc and miR-586.
Keyphrases
- long non coding rna
- poor prognosis
- endothelial cells
- binding protein
- protein protein
- high glucose
- signaling pathway
- amino acid
- cell proliferation
- transcription factor
- genome wide
- electronic health record
- small molecule
- diabetic rats
- high intensity
- drug induced
- long noncoding rna
- gene expression
- dna methylation
- oxidative stress
- nucleic acid
- stress induced